urinary incontinence mohammad

urinary frequency is micturition more than _____ times per day

8

nocturia is more than ______ void(s) per night

1

which gender and age is most affected by urinary incontinence

women during menopause (almost 2x than men)

describe the normal physiology of how urine is releases

muscles/receptors/etc

to urinate:

detrusor contraction= M3

urethral relaxation= no adrenergic stim

inhibit urine:

detrusor relaxation= B3

urethra= a1

which receptor(s) would result in urine inhibition

detrusor= B3

urethra=a1

which receptor would result in urination

detrusor= M3

urethral relaxation= no adrenergic stim

STRESS INCONTINENCE

etiology/receptors

s/s

- urethra not closing/weak (a1)

- when intra abdominal pressure increases

- small amounts of urine lost during activity, sneeze, cough, laugh

-no incontinence when sleeping/resting!

STRESS INCONTINENCE

risk factors

pregnancy

child birth

menopause

age

(remember this is bc of a weak urethra-> urine leaks out during activity)

Urge incontinence (OAB)

etiology/receptors

s/s

- bladder is overactive/ detrusor is contracting (M3)

urgency, frequency, nocturia

urge incontinence

risk factors

age, neurologic disease

(this is when detrusor contracts even if bladder isnt full)

overflow incontinence

etiology

s/s

- urethra overactive (closes)

- bladder underactive (relaxed)

overfilled bladder that cant empty= leaks out

-sense of fullness, incomplete bladder emptying, frequency, straining

overflow incontinence

risk factors

bladder outlet obstruction (BPH)

spinal cord injuries

pelvic surgery

mixed incontinence

etiology

bladder is overactive (contracting) and urethra is underactive (not closing)

mix of stress (urethra) and urge (bladder overactive)

what is mixed UI a combo of

stress (weak urethra) and urge (detrusor contracting)

functional incontinence

etiology

risk factors

physiology is normal, but underlying disease (ex: dementia, immobile) prevents reaching toilet in time

risk factors: cognitive impairment, musculoskeletal limitations

how can overflow incontinence be diagnosed

measure amount of urine left in bladder after normal urination

normal: <50

repeat: 50-100

dysfunction: >200ml

what is first line therapy for UI

non-pharm

what lifestyle modifications should be recommended to pts with UI

- smoking cessation

- avoid caffeine and alcohol

- weight loss

- prevent constipation

other than lifestyle modifications, what non pharm tx is recommended for UI

- toilet scheduling: schedule time to go, increase time btwn breaks

- pelvic floor muscle exercises/Kegel: squeeze like youre trying to stop urine

which drugs can make all types of UI worse by increasing overall urination

- diuretics

- SGLT2 inhibitors (jardiance)

which drugs can make functional incontinence worse and why

impair cognition

- opioids

-benzos

- antipsychotics

- anticholinergics

which drugs make stress incontinence worse and how

relax urethra: alpha-1 antagonist (terazosin)

induce cough: ACE inhibitors

which drugs make overflow incontinence worse and how

relax detrusor(B3 or block M3): calcium channel blockers

anticholinergics/psychotics,

TCAs,

skeletal muscle relaxants

contract urethra(a1):

adrenergic agonist (pseudoephedrine),

alpha agonists (clonidine),

beta blockers

which drugs make urge/OAB worse and how

make detrusor contract (M3 ag)

cholinesterase inhibitors (donepezil)

bethanechol

functional UI

pharm tx:

no pharm agents. must remove underlying cause (why is there cognitive barrier?)

stress urinary incontinence

pharm tx:

remember due to weak urethra.

1. local estrogens

- estrogen vaginal cream 0.5g 3x weekly

- estradiol vaginal ring q3months

2. a1 agonists (to contract urethra)

- pseudoephedrine 15-60mg tid

- phenylephrine 10mg qid

3. duloxetine (in europe) bc NE reuptake inhibitor

when can local estrogens be used to treat UI?

mech?

examples?

AE?

stress incontinence to strengthen urethra

mech: increase thickness of urethral tissue/tone

- estrogen vaginal cream or ring

AE: vaginal spotting, breast tenderness, nausea

when can a1 agonists be used to treat UI?

examples?

AE?

CI?

stress incontinence to contract urethra (a1)

-pseudoephedrine, phenylephrine

AE: dizziness, increased bp, insomnia, headache

CI: HTN, arrythmias, CAD

t/f: a combination of local estrogens and a1 agonists may be more effective than monotherapy for stress UI

true

pharm tx for overflow incontinence

usually only non pharm

1. treat underlying obstruction (ex: BPH)

2. bethanechol (M3 contraction)

3. catheterization

pharm tx for urge UI/ OAB

problem is constant detrusor contractions (need M3 block or B3 stim)

1. anticholinergic/ antimuscarinic (m3)

-oxybutynin, tolterodine, fesoterodine, darifenacin, solifenacin, trospium

2. b3 agonists

- mirabegron, vibegron

which formulations for anticholinergics have the most side effects? least?

(most) IR> ER> topical (least)

where are M1, M2, and M3 receptors found? which AE are prominent due to blockade?

M1= nerves, salivary gland

- dizzy, impaired memory/cognition, dry mouth

M2= detrusor, heart, GI

- relax bladder, tachycardia, QT, constipation

M3= detrusor, salivary gland, GI

- relax bladder, dry mouth, constipation

which antimuscarinic agents can treat OAB? which have better tolerability due to greater affinity for M3?

agents: oxybutynin, tolterodine, fesoterodine, darifenacin, solifenacin, trospium

better= darifenacin, solifenacin, trospium

oxybutynin

use?

tolerability?

Ditropan

antimuscarinic for OAB

reduces detrusor contractions but also blocks salivary glands (dry mouth)

-most difficult one to tolerate!

why is oxybutynin ER and gel better tolerated than IR

ER has less first pass and less of the active metabolite. Gel bypasses the liver altogether= less active metabolite

tolterodine

Detrol

antimuscarinic for OAB

- better than oxybutynin bc less lipophilic so less reaches brain

fesoterodine

Toviaz

antimuscarinic for OAB

-this is prodrug of tolterodine, less side effects

darifenacin

Enablex

blocks M3, for OAB

more selective= better tolerated

solifenacin

vesicare

blocks M3, for OAB

more selective= better tolerated

trospium

Sanctura

blocks M3, for OAB

more selective= better tolerated

which B3 agonists are used for OAB

mirabegron (myrbetriq)

vibegron (Gemtesa)

t/f: combining an antimuscarinic and b3 agonist is more effective than monotherapy for OAB

false

after how long should you consider switching to another agent if the first one isnt working

8-12 weeks (up to 3 months)